Prohibitin is involved in mitochondrial biogenesis in plants

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dc.contributor.authorC S Ahn-
dc.contributor.authorJeong Hee Lee-
dc.contributor.authorA R Hwang-
dc.contributor.authorW T Kim-
dc.contributor.authorH S Pai-
dc.date.accessioned2017-04-19T09:06:30Z-
dc.date.available2017-04-19T09:06:30Z-
dc.date.issued2006-
dc.identifier.issn0960-7412-
dc.identifier.uri10.1111/j.1365-313X.2006.02726.xko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7760-
dc.description.abstractProhibitin, which consists of two subunits PHB1 and PHB2, plays a role in cell-cycle progression, senescence, apoptosis, and maintenance of mitochondrial function in mammals and yeast. In this study, we examined the role of prohibitins in plants by using virus-induced gene silencing (VIGS) of two prohibitin subunit genes of Nicotiana benthamiana, designated NbPHB1 and NbPHB2. NbPHB1 and NbPHB2 were targeted to the mitochondria, and their gene expression was suppressed during senescence. VIGS of NbPHB2 caused severe growth inhibition, leaf yellowing and symptoms of cell death, whereas VIGS of NbPHB1 resulted in a milder phenotype. At the cellular level, depletion of these subunits affected mitochondria by severely reducing their number and/or mass, and by causing morphological and physiological abnormalities. Suppression of prohibitin function resulted in a 10- to 20-fold higher production of reactive oxygen species and induced premature leaf senescence. Finally, disruption of prohibitin function rendered the plants more susceptible to various oxidative stress-inducing reagents, including H2O2, paraquat, antimycin A and salicylic acid. These results suggest that prohibitins play a crucial role in mitochondrial biogenesis and protection against stress and senescence in plant cells.-
dc.publisherWiley-
dc.titleProhibitin is involved in mitochondrial biogenesis in plants-
dc.title.alternativeProhibitin is involved in mitochondrial biogenesis in plants-
dc.typeArticle-
dc.citation.titlePlant Journal-
dc.citation.number4-
dc.citation.endPage667-
dc.citation.startPage658-
dc.citation.volume46-
dc.contributor.affiliatedAuthorJeong Hee Lee-
dc.contributor.alternativeName안창숙-
dc.contributor.alternativeName이정희-
dc.contributor.alternativeName황아름-
dc.contributor.alternativeName김우택-
dc.contributor.alternativeName배현숙-
dc.identifier.bibliographicCitationPlant Journal, vol. 46, no. 4, pp. 658-667-
dc.identifier.doi10.1111/j.1365-313X.2006.02726.x-
dc.subject.keywordmitochondrial morphology-
dc.subject.keywordreactive oxygen species-
dc.subject.keywordsenescence-
dc.subject.keywordstress tolerance-
dc.subject.keywordvirus-induced gene silencing-
dc.subject.localmitochondrial morphology-
dc.subject.localROS-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localsenescence-
dc.subject.localSenescence-
dc.subject.localStress tolerance-
dc.subject.localstress tolerance-
dc.subject.localvirus-induced gene silencing-
dc.subject.localVIGS-
dc.subject.localVirus-induced gene silencing-
dc.subject.localVirus-induced gene silencing (VIGS)-
dc.description.journalClassY-
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